Infectious Pancreatic Necrosis

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Caused By: Infectious Pancreatic Necrosis Virus – IPNV


Infectious Pancreatic Necrosis (IPN) is a fish disease caused by an unenveloped icosahedral birnavirus. The IPN virus is the type species of the genus Aquabirnavirus. It is highly contagious and mainly affects intensively reared salmonid species although it has a wide host range.

The virulence of IPNV isolates varies widely; while most are isolated from subclinical cases, some isolates can produce very high fish mortality.

This disease is not zoonotic.


Worldwide, including North and South America, Europe. Asia and Oceania.

Due to increased awareness, regulations on movement of fish eggs and hygiene policies, many US states and provinces have successfully reduced or eradicated the disease from their fisheries. Unfortunately the situation in Europe is not so positive and disease is widespread. Iceland has no IPN infection in salmonids despite their large scale production probably and extensive fish inspection procedures. This may be due to their very strict importation policy for fin fish and may be an example to follow.

The virus is transmitted horizontally via shared water. It is shed in both faeces and urine. Brook and rainbow trout can also transmit disease vertically and this may be a feature in other species too. Homeothermic vertebrates and invertebrates are thought to be a source of the virus early in some outbreaks. The virus can also be transmitted mechanically by fomites and personnel.


Although salmonid species are by far the most common and economically important, a huge range of fish can be infected by IPN including Japanese eels, milkfish, pike, menhaden, wrasse, halibut, scallops and clams. The host range of the virus is difficult to monitor due to the isolation of many other widespread birnaviruses that are difficult to differentiate from IPNV.

The disease most characteristically presents in rainbow trout, brook trout, brown trout, atlantic salmon and several pacific salmon species.

Susceptibility generally decreases with age and resistance is usually reached by 1500 degree days. This does of course mean that water temperature will dictate the speed at which fish are granted immunity to IPN.

Atlantic salmon smoults can be affected when first transferred to sea water from fresh water.

Clinical Signs

Affected fish darken in colour, stop feeding, exhibit a pronounced distension of the abdomen and often swim in spirals or corkscrew manoeuvres. Pinpoint haemorrhages are visible on the skin and fins. Exophthalmia is often a feature.

The first sign of an outbreak in salmonid fry is a sudden increase in daily mortality which progressively increases. Faster growing fish will usually be affected first, increasing the economic impact of the disease. Cumulative mortality varies from 10% to >90%.

Disease course is usually only 1-2 weeks in individual fish, after which surviving fish recover.


Virus can be consistently detected using cell cultures from teleost cell lines. It can then be confirmed by serum neutralisation or ELISA . IPNV antigens can be detected in tissues by indirect fluorescent antibody testing.

On post-mortem, the pancreas has white-grey necrotic patches throughout and petechiation is evident throughout the viscera.

Microscopically, focal necrosis of the acinar and islet cells and also of the haematopoietic tissue of the kidney can be seen. Typical viral particles with an icosahedral shape can be seen cytoplasmically within affected cells.

In carrier animals, high titres of virus can be isolated from the viscera and necrosis is seen in the lamina propria of the intestine.


There is no treatment for infected fish – disease has a short course and once mortalities have waned, survivors will recover.

Reduction of population density may help to reduce mortality during an outbreak.


Control is difficult due to the ubiquitous nature of the virus and thus control policies must be strictly adhered to and hygiene practices followed exclusively. Unfortunately, the economic losses from slaughter policies and movement restrictions are often larger than those caused directly by the disease itself.

Fertilised eggs should not be introduced if from broodstock of questionable IPN status. If possible, a protected water supply such as a spring or borehole pond where no fish ingress is possible should be used. Infected broodstock in which the virus is isolated should be destroyed.

Disinfection of eggs is unfortunately not always successful but may have some value.

Vaccines are available that are designed for atlantic salmon smoults after sea transfer but results are unreliable at present.

Mixing populations, unhygienic or stressful transport and size of smolts at transfer are all risk factors for IPN which must be monitored and strictly controlled.

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Munro, E.S. and Midtlyng (2011). Infectious Pancreatic Necrosis and Associated Aquatic Birnaviruses. In: Fish Diseases and Disorders, Volume 3, 2nd edition (eds. P.T.K. Woo and D.W. Bruno), CABI, Wallingford, UK. pp. 1-65.


This article was originally sourced from The Animal Health & Production Compendium (AHPC) published online by CABI during the OVAL Project.

The datasheet was accessed on 31 July 2011.

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